Abstract: CP violation in neutral B meson oscillations is an experimental observable that could be directly related to the baryon asymmetry of the Universe through the B-mesogenesis mechanism. As this phenomenon is highly suppressed in the Standard Model, it could also be a sensitive probe for many new physics scenarios that modify neutral meson mixing. Motivated by these facts, and the timely B physics program at the LHC and Belle II, we analyze how large CP violation in the mixing of neutral Bd and Bs meson systems could be. We answer this question, in light of current experimental data, within three different scenarios, namely: (i) generic heavy new physics only affecting the mass mixing Mq12, (ii) vectorlike quark extensions that introduce deviations of 3 x 3 CKM unitarity, and (iii) light new physics modifying the decay mixing Gamma q12. We find that enhancements of the semileptonic asymmetries, that measure the amount of CP violation in mixing, at the level of 10-3 for the Bd system and 10-4 for the Bs system can be achieved within scenarios (i) and (ii), while they are much more suppressed in realistic UV completions triggering scenario (iii). With respect to cosmology, the difficulty of finding large CP asymmetries in our analysis puts the B-mesogenesis mechanism in tension. Finally, we conclude that upcoming experimental searches for CP violation in B meson mixing at LHCb and Belle II are unlikely to detect a new physics signal for the most generic models.

Abstract: The immune system should constitute a strong selective pressure promoting viral genetic diversity and evolution. However, HIV shows lower sequence variability at T-cell epitopes than elsewhere in the genome, in contrast with other human RNA viruses. Here, we propose that epitope conservation is a consequence of the particular interactions established between HIV and the immune system. On one hand, epitope recognition triggers an anti-HIV response mediated by cytotoxic T-lymphocytes (CTLs), but on the other hand, activation of CD4(+) helper T lymphocytes (T-H cells) promotes HIV replication. Mathematical modeling of these opposite selective forces revealed that selection at the intrapatient level can promote either T-cell epitope conservation or escape. We predict greater conservation for epitopes contributing significantly to total immune activation levels (immunodominance), and when T-H cell infection is concomitant to epitope recognition (transinfection). We suggest that HIV-driven immune activation in the lymph nodes during the chronic stage of the disease may offer a favorable scenario for epitope conservation. Our results also support the view that some pathogens draw benefits from the immune response and suggest that vaccination strategies based on conserved T-H epitopes may be counterproductive.